The objective of this project is to develop a method for selectively producing intracerebral hematomas in basal ganglia and deep structures, sparing cortex. As developed originally in dogs, a technique utilizing Microfil (R) silicone latex cylinders injected into the internal carotid artery was adapted to the monkey. Randomly certain animals showed intracerebral hematomas contiguous with zones of deep infarction. This was thought to be a preterminal emiphenomenon related to the hypertension reputedly caused by ketamine. Further testing of the hypothesis of Globus, that hematoma, hemorrhagic infarction and ischemia represent a continuum of pathophysiologic events following ischemia, animals were stressed in acute and chronic phases after embolism with a) ketamine, b) hypercapnia, c) norepinephrine and d) angiotensin. Chronic animals stressed with hypercapnia regularly developed intracranial hematomas distal to the site of vascular occlusion. Other stress agents tested produce more extensive infarction in acute animals compared to nonstressed controls and hemorrhagic infarctions in chronic animals. These findings indicate that: 1. Hemorrhage developed during the vasoproliferative phase of ischemia injury (5-6 days); 2. During vasodilation (hypercapnia) and 3. Progressed from the collaterally supplied peri-infarction area into the necrotic core.